In a breakthrough, scientists have found a way to postpone several signs of aging in mice.

Their method could pave the way for the development of similar techniques to halt or delay wrinkles, cataracts, muscle wasting and other age-related disorders in humans.

Researchers at the Mayo Clinic in Rochester, Minn., found the key was in a specific type of cell that builds up in our tissues as we age: senescent cells.

Senescent cells act differently from young, healthy cells, which divide continuously, helping to maintain the proper functioning of body tissues and organs. In contrast, senescent cells have stopped dividing. Although we produce senescent cells throughout our lives, our bodies are less able to clear them from our bodies as we age, so they build up in tissue.

The researchers used a drug to kill senescent cells and found that doing so improved the condition of the tissues holding those cells, thereby halting or preventing age-related disorders.

The finding was significant for several reasons. It was the first time that research showed that senescent cells can drive the aging process in the tissues in which they collect, said the New York Times.

Additionally, "If you could clear senescent cells, you perhaps could treat age-related diseases as a group rather than individually," Jan van Deursen, the paper's senior author and a Mayo Clinic professor, said to the Wall Street Journal.

He and his team published their results in the November 3 issue of Nature.

How the experiments worked

The researchers used mice who had been genetically engineered to age quickly and die of heart attacks at an early age, no matter how healthy their tissues. So, the experiments could not affect how long the mice lived. However, both studies did show that targeting senescent cells could improve health in old age.

In the first experiment, Dr. van Deursen injected the mice over their lifetimes with a drug that would cause senescent cells to self-destruct. He found "quite a dramatic delay" in age-related developments in the mice, such as cataracts and changes to muscles and fat.

In the second experiment, Dr. van Deursen used the senescent cell-clearing drug on mice that had already reached middle age and developed cataracts. While the cataracts did not disappear, signs of aging in fat and muscle were delayed.

Although these mice died early as they were genetically programmed to do, their old age was healthier than it would have been otherwise.

Note that the mice in this study didn’t live any longer; they just spent more of their life being healthy. That is an incredibly important distinction and one that scientists who work on ageing are starting to bear in mind. James Kirkland, one of the study’s leaders, says, “Until two or three years ago, the basic biology was focused on lifespan. Increasingly, it’s become more focused on increasing healthspan too. People may want to live longer but they don’t want to live longer at all costs. They want to live more healthily. Older people value independence and the ability to carry out the activities of daily life.”

Next steps

The researchers plan to conduct experiments on senescent cells in mice who age normally to see if they live longer. They will also look at how often senescent cells should be cleared out: frequently or intermittently, such as once a year.

Another question is whether this technique could increase cancer risk. Senescence helps prevent cancer, because it keeps cells from dividing uncontrollably. If senescent cells were removed, it's unclear whether tumors would proliferate.

Killing off senescent cells might also cause the loss of other benefits they provide: For instance, they may keep infections in check or repair skin wounds.

Still, the discovery of senescent cells' role in the aging process is significant:

“People used to see aging as a rusting nail — there’s nothing you can do about it,” [Dr. Judith Campisi of the Buck Institute for Research on Aging] said. “But we now know that there are processes that are driving aging, and that those processes can be meddled with.”